Their homologs are significantly mutated (SRCAP in prostate cancer and glioblastoma; CLASPIN in gliomas and breast cancer) or overexpressed (H2A.Z in liver, colorectal, and metastatic breast cancer) in human cancers, and these alterations are predicted to play important roles in carcinogenesis66–71. This evidence concerns the gene CLSPN and Familial prostate cancer.